Comparative effects of University of Wisconsin and Euro-Collins solutions on pulmonary mitochondrial function after ischemia and reperfusion.
BACKGROUND
The aim of this study was to compare the effects of Euro-Collins and University of Wisconsin solutions on pulmonary mitochondrial function after cold ischemia and subsequent warm reperfusion.


METHODS
Seventeen pigs underwent lung harvesting after classical lung flush with either University of Wisconsin or Euro-Collins solutions. The mitochondria were isolated from fresh swine lungs, from swine lungs subjected to 24 hr of cold ischemia, and from swine lungs subjected to 24 hr of ischemia followed by 30 min of subsequent ex vivo reperfusion at 37 degrees C with Krebs-Henseleit buffer solution and air ventilation. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption rates. During reperfusion, the lung function was assessed by the pulmonary aerodynamic parameters and the pulmonary vascular resistance.


RESULTS
Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain. However, the yield of oxidative phosphorylation was conserved. After reperfusion, pulmonary mitochondria underwent a significant worsening in the oxidoreductase activities of the respiratory chain, and a decrease in the respiratory control and the efficiency of oxidative phosphorylation. Meanwhile, the reperfused lungs showed evidence of early dysfunction, assessed by the aerodynamic parameters and pulmonary vascular resistance. In this model, there was no advantage of University of Wisconsin solution over Euro-Collins solution.


CONCLUSIONS
The mild mitochondrial alterations after cold ischemia were not sufficient to explain the limited tolerance of lung to ischemia. After reperfusion, the mitochondrial damage was more severe and could be involved in the posttransplant lung dysfunction.
Detry
O
O
Department of Surgery and Transplantation, University Hospital of Liège, Belgium.
Willet
K
K
Lambermont
B
B
Meurisse
M
M
Pincemail
J
J
Serteyn
D
D
Lamy
M
M
Defraigne
J O
JO
Limet
R
R
Sluse
F E
FE
D000241:Adenosine / Q000494:pharmacology; D000493:Allopurinol / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D005260:Female; D005978:Glutathione / Q000494:pharmacology; D006982:Hypertonic Solutions / Q000494:pharmacology*; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology; D008168:Lung / Q000098:blood supply* / Q000187:drug effects* / Q000648:ultrastructure; D008297:Male; D008928:Mitochondria / Q000187:drug effects*; D019188:Organ Preservation Solutions / Q000494:pharmacology*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D010766:Phosphorylation; D011887:Raffinose / Q000494:pharmacology; D015424:Reperfusion; D013552:Swine; D014655:Vascular Resistance
C037096:Euro-Collins' solution; D006982:Hypertonic Solutions; D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose